The present invention relates to the field of cardiac surgery, and more particularly to the field of prosthetic heart valves, especially prosthetic mitral valves.
The human heart 10, depicted in cross-sectional long axis view in FIG. 1A (during diastole) and 1B (during systole), is a muscular organ that pumps deoxygenated blood through the lungs to oxygenate the blood and pumps oxygenated blood to the rest of the body by rhythmic contractions of four chambers.
After having circulated in the body, deoxygenated blood from the body enters right atrium 12 through vena cava 14. Right atrium 12 contracts, pumping the blood through a tricuspid valve 16 into right ventricle 18, FIG. 1A. Right ventricle 18 contracts, pumping the blood through a pulmonary semi-lunar valve 20 into the pulmonary artery 22 which splits to two branches, one for each lung, FIG. 1B. The blood is oxygenated while passing through the lungs and reenters the heart to the left atrium 24. Left atrium 24 contracts, pumping the oxygenated blood through the mitral valve 26 into the left ventricle 28, FIG. 1A. Left ventricle 28 contracts, pumping the oxygenated blood through the aortic valve 30 into the aorta 32 to be distributed to the rest of the body, FIG. 1B.
In mitral valve 26, an approximately circular mitral annulus 34 defines a mitral valve orifice 36. Attached to the periphery of mitral annulus 34 is an anterior leaflet 38 and a smaller posterior leaflet 40, leaflets 38 and 40 connected to papillary muscles 44 at the bottom of left ventricle 28 by chordae 46. The typical area of the mitral lumen in a healthy adult is between 4 and 6 cm2 while the typical total surface area of leaflets 38 and 40 is significantly larger, approximately 12 cm2.
During diastole depicted in FIG. 1A, left atrium 24 contracts to pump blood into left ventricle 28 through orifice 36 of mitral valve 26. The blood flows through orifice 36, pushing leaflets 38 and 40 into left ventricle 28 with little resistance. The leaflets of aortic valve 30 are kept closed by blood pressure in aorta 32.
During systole, depicted in FIG. 1B, left ventricle 28 contracts to pump blood into aorta 32 through aortic valve 30 which leaflets are pushed open by the blood flow with relatively little resistance. Mitral annulus 34 contracts, pushing leaflets 38 and 40 inwards and reducing the area of mitral valve orifice 36 by about 20% to 30%. Papillary muscles 44 contract, maintaining the tension of chordae 46 and pulling the edges of leaflets 38 and 40, preventing prolapse of leaflets 38 and 40 into left atrium 24. Leaflets 38 and 40 curve into left ventricle 28 and coapt to accommodate the excess leaflet surface area, producing a coaptation surface 42 that constitutes a seal. The typical length of coaptation surface 42 in a healthy heart 10 of an adult is approximately 7-8 mm. The pressure of blood in left ventricle 28 pushes against the ventricular surfaces of leaflets 38 and 40, tightly pressing leaflets 38 and 40 together at coaptation surface 42 so that a tight leak-proof seal is formed.
An effective seal of mitral valve 26 during ventricular systole is dependent on a sufficient degree of coaptation, in terms of length, area and continuity of coaptation surface 42. If coaptation surface 42 is insufficient or non-existent, there is mitral valve insufficiency, that is, regurgitation of blood from left ventricle 28 into left atrium 24 during ventricular systole. A lack of sufficient coaptation may be caused by any number of physical anomalies that allow leaflet prolapse (e.g., elongated or ruptured chordae 46, weak papillary muscles 44) or prevent coaptation (e.g., short chordae 46, small leaflets 38 and 40). There are also pathologies that lead to a mitral valve insufficiency including collagen vascular disease, ischemic mitral regurgitation (resulting, e.g., from myocardial infarction, chronic heart failure, or failed/unsuccessful surgical or catheter revascularization), myxomatous degeneration of leaflets 38 and 40 and rheumatic heart disease. Mitral valve insufficiency leads to many complications including arrhythmia, atrial fibrillation, cardiac palpitations, chest pain, congestive heart failure, fainting, fatigue, low cardiac output, orthopnea, paroxysmal nocturnal dyspnea, pulmonary edema, shortness of breath, and sudden death.
Apart from humans, mammals that suffer from mitral valve insufficiency include horses, cats, dogs, cows, sheep and pigs.
It is known to use open-heart surgical methods to treat mitral insufficiency, for example by modifying the subvalvular apparatus (e.g., lengthening or shortening chordae 46) to improve leaflet coaptation, implanting an annuloplasty ring to force mitral valve annulus 34 into a normal shape.
Aortic valves are known to suffer from aortic insufficiency or aortic stenosis. It is known to deploy a prosthetic aortic valve using minimally invasive surgery to replace a malfunctioning native aortic valve. Typically, an expandable frame (e.g., a stent or a ring) supporting artificial aortic leaflets is positioned inside the orifice of an aortic valve, typically endovascularly with a catheter passing through the aorta, but also transapically through a hole near the apex of the heart, passing into left ventricle 28. The frame is expanded across the aortic annulus folding and overlying the native aortic valve leaflets, maintaining the prosthetic aortic valve in place by exertion of an axial force and by adopting an “hourglass” shape that distributes axial forces on the native aortic valve annulus and the surrounding tissue. Commercially available prosthetic aortic valves include the Lotus™ by Sadra Medical (Campbell, Calif., USA) and the CoreValve™ by Medtronic (Minneapolis, Minn., USA).
It has been suggested to deploy a prosthetic mitral valve, analogous to a prosthetic aortic valve. A challenge to implementing such suggestions is retention of the prosthesis in place during ventricular systole. Unlike the aortic valve annulus that constitutes a stable anchoring feature, especially when calcified, the mitral valve annulus is not a sufficiently stable anchoring feature (less than half of the mitral valve annulus is of fibrotic tissue) and is dynamic (changing size and shape as the heart beats). Further, unlike the aortic valve that is open during ventricular systole, the mitral valve must withstand the high pressures in the left ventricle caused by contraction of the left ventricle during ventricular systole, pressures that tend to force a mitral valve prosthesis deployed across a mitral valve annulus into the left atrium.
Additional background art includes US Application No. 2011/0137397 by Chau et al., which discloses “Embodiments of prosthetic valves for implantation within a native mitral valve are provided. A preferred embodiment of a prosthetic valve includes a radially compressible main body and a one-way valve portion. The prosthetic valve further comprises at least one ventricular anchor coupled to the main body and disposed outside of the main body. A space is provided between an outer surface of the main body and the ventricular anchor for receiving a native mitral valve leaflet.”